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I&I WC2 > Clinical pharmacology III > Flashcards

Clinical pharmacology III Flashcards

(48 cards)

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1
Q

What are the two main causes of chronic kidney disease?

A
  1. Diabetes
  2. Hypertension
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2
Q

How can glomerular kidney disease present itself? (2)

A
  1. Nephrotic
  2. Nephritic
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3
Q

What are the characteristics of nephrotic syndrome? (4)

A
  1. Fatty urine casts
  2. Proteinuria > 3.5 g/day
  3. Hematuria +/-
  4. Kidney disease, without primarily inflammation
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4
Q

What are the clinical features of nephrotic syndrome? (3)

A
  1. Generalized edema
  2. Periorbital edema
  3. HTN
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5
Q

What are the characteristics of nephritic syndrome? (3)

A
  1. RBC casts
  2. Proteinuria < 3.5 g/day
  3. Inflammation of the glomerulus
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6
Q

What are the clinical features of nephritic syndrome? (2)

A
  1. HTN
  2. Edema
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7
Q

What are examples of primary glomerular kidney diseases? (5)

A
  1. Minimal change disease
  2. Primary focal- and segmental glomerulosclerosis
  3. Membranous nephropathy
  4. Membranoproliferative glomerulonephritis
  5. IgA nephropathy
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8
Q

What are examples of secondary glomerular kidney diseases? (6)

A
  1. Lupus nephritis
  2. Anti-GBM disease
  3. Amyloidosis
  4. Infection-related GN
  5. ANCA-associated vasculitis
  6. Atypical HUS
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9
Q

Which factors can you measure in a blood test to determine if someone has glomerular kidney disease? (5)

A
  1. Anti-nuclear antibodies (ANA)
  2. Anti-neutrophil cytoplasmic antibodies (ANCA)
  3. Anti-GBM antibodies
  4. Complement C3 and C4
  5. Underlying disease: M protein, virology
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10
Q

What is the most common cause of nephrotic syndrome? Due to what?

A

Membranous nephropathy -> due to anti-PLA2R antibodies

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11
Q

What are the histopathological features of membranous nephropathy?

A

Subepithelial deposits (Spikes) on top of GBM and podocytes are fused

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12
Q

Membranous nephropathy: what are the subepithelial deposits (spikes) visual on EM most likely?

A

Antibody/immune complexes

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13
Q

What is the role of M-type phospholipase A2 receptor in membranous nephopathy?

A

Target antigen

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14
Q

Where is M-type phospholipase A2 receptor present?

A

Podocytes

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15
Q

True or false: patients have antibodies against the M-type phospholipase A2 receptor

A

True

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16
Q

What are the steps in the pathogenesis of membranous nephropathy? (4)

A
  1. Immune complex formation in kidney
  2. Complement activation
  3. Damage of podocytes
  4. Proteinuria
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17
Q

Which two processes can lead to autoimmunity in membranous nephropathy?

A
  1. Processing of PLA2R antigen into soluble form
  2. Endocytosis of PLA2R antigen
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18
Q

How does processing of PLA2R antigen into soluble form lead to autoimmunity in membranous nephropathy? (6)

A
  1. Antigen binding to autoreactive B cell
  2. Antigen fragmentation
  3. Antigen uptake and presentation to T cell
  4. Cytokine released from stimulated T cells
  5. Affinity maturation/CSR
  6. Increased frequency of autoreactive B cells occurring over time
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19
Q

How does endocytosis of PLA2R antigen lead to autoimmunity of membranous nephropathy?

A
  1. APCs take up antigen
  2. Co-
  3. Affinity maturation/CSR
  4. Increased frequency of autoreactive B cells occurring over time
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20
Q

What is the prognosis of glomerular disease?

Study These Flashcards
A

75-100% survival after 15 years depending on the disease

21
Q

Which patients are at a higher risk of a bad prognosis for glomerular kidney disease? (3)

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A
  1. > 3.5gr/day
  2. Decrease of kidney function at baseline
  3. Male
22
Q

Why do you definitely start treatment of higher risk glomerular kidney patients?

Study These Flashcards
A

To prevent progression to end-stage kidney disease

23
Q

What are treatment options for kidney disease to prevent kidney failure? (2)

Study These Flashcards
A
  1. Dialysis
  2. Kidney transplantation
24
Q

Which cells can you target to combat the autoimmune part of membranous nephropathy? (3)

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A
  1. Targeting T cells and cytokines
  2. Targeting APCs and T cells
  3. Targeting B cells, plasma cells and complement
25
True or false: kidney disease patients treated with rituximab have a better outcome than kidney disease patients treated with cyclosporine
True
26
Kidney disease patients: If rituximab doesn't work, what kind of treatment do you give these patients? (2)
1. Cyclophosphamide (chemo) 2. Prednison
27
What can be a side-effect of treating kidney disease patients with rituximab or cyclosporine?
Kaposi sarcoma
28
What is a hallmark of hemolytic uremic syndrome (HUS)?
Thrombotic microangiopathy
29
What are the characteristics of thrombotic microangiopathy? (3)
1. Hemolysis 2. Lack of thrombocytes 3. Decrease kidney function
30
What are the three main characteristics of HUS?
1. Microangiopathic hemolytic anemia 2. Thrombocytopenia 3. Acute kidney injury
31
What does microangiopathic hemolytic anemia entail? (2)
1. Small vessel disease 2. Destruction of red blood cells
32
How does the destruction of red blood cells in microangiopathic hemolytic anemia look when studying a biopsy?
1. Narrowing of red arterioles 2. Endothelium of capillaries are swollen (activation of endothelium)
33
What are the four underlying diseases leading to HUS?
1. Infection-induced HUS 2. HUS with coexisting diseases or conditions 3. Cobalamin C defect- HUS 4. Atypical HUS
34
What are the four types of infection-induced HUS?
1. S.pneumoniae-HUS 2. STEC-HUS 3. Influenza A, H1N1 4. HIV
35
When does infection-induced HUS occur?
Comes in outbreaks (poisoned food)
36
What are examples of HUS with coexisting diseases or conditions? (6)
1. HSCT/solid organ transplantation 2. AID 3. Malignancy 4. Drugs 5. Malignant hypertension 6. Pre-existing nephropathy
37
What causes atypical HUS?
Complement regulation disorder
38
What are the three types of atypical HUS?
1. DGKE-HUS 2. HUS with dysregulation of the complement alternative pathway 3. HUS without identified complement or DGKE mutation or anti-CFH antibody
39
What underlying mechanisms cause HUS with dysregulation of the complement alternative pathway?
1. Mutations in CGH, CFI, MCP, C3, CFB, THBD 2. Anti-CFH antibody
40
Complement: all three pathways lead to? (3)
1. Inflammation 2. Membrane attack complex 3. Opsonization
41
Eventueel complement pathway specifics
42
What do the membrane attack complex and/or C5a activate/induce in atypical HUS?
1. WIth C5a: activation of platelets 2. RBC lysis 3. Endothelial cell damage 4. C5a: induces clot formation
43
HUS: What can go wrong in regulation? (2)
1. Gene mutations (C regulating genes) 2 Anti-factor H antibodies
44
Which gene mutations can occur in HUS? (4)
1. Factor H,I (soluble) 2. CD46/MCP (membrane bound) 3. C3, GOF (factor H binding, soluble) 4. Factor B (soluble)
45
HUS: How do you treat patients if there is something wrong in the regulation of complement?
1. Plasma exchange 2. Kidney transplantation 3. Eculizumab/ravulizumab
46
HUS: When is there a risk of recurrence after kidney transplantation?
If a soluble factor is still present after Tx
47
Where does eculizumab (anti-CD5) interfere in the alternative pathway?
Prevents C5 cleavage and MAC formation
48
What is the downside of eculizumab?
Expensive

I&I WC2 (16 decks)

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